A comparison of UVb compact lamps in enabling cutaneous vitamin D synthesis in growing bearded dragons

    loading  Checking for direct PDF access through Ovid

Excerpt

The bearded dragon (Pogona vitticeps) is one of the most frequently kept reptile species in North America (Wright, 2008) and possibly in Europe. The most common disorders in captive P. vitticeps belong to the metabolic bone disease (MBD) complex (Wright, 2008). This complex of diseases includes rickets, osteoporosis and secondary hyperparathyroidism and is caused by an imbalance of calcium and/or phosphorus in the body (Divers & Mader, 2005). Vitamin D3 regulates calcium metabolism by inducing intestinal absorption and renal reabsorption of Ca and P (Ajibade, Benn, & Christakos, 2010; Haxhiu et al., 2014). Furthermore, a misbalance in dietary vitamin D, Ca or P intake can cause renal disease in lizards (Miller, 1998), which leads to increased plasma levels of P and uric acid (Knotek, Hauptman, Knotkova, Hajkova, & Tichý, 2002).
Vitamin D3 deficiency can result in hypocalcaemia, which in turn can lead to development of MBD (Holick, Tian, & Allen, 1995). Vitamin D3 can either be provided exogenously or endogenously synthesized in the skin. The epidermal cells of the skin contain 7‐dehydrocholesterol (7‐DHC) which is transformed to pre‐vitamin D3 when exposed to ultraviolet b (UVb) radiation between 290 and 320 nm (Fraser, 1995). Pre‐vitamin D3 is isomerized to vitamin D3 in a thermally dependent step (Holick et al., 1980). Vitamin D3 in the skin binds to vitamin D‐binding protein (VDBP) which transports it into the bloodstream. Vitamin D3 is hydroxylated in the liver to 25(OH)D3, which again binds to VDBP and re‐enters the circulation. Circulating 25(OH)D3 is regarded as the primary storage form of vitamin D3 and is used to assess vitamin D3 status (Gillespie, Frye, Stockham, & Fredeking, 2000; Holick, 1990). 25(OH)D3 is metabolized by renal cells to the active endocrine hormone, 1,25(OH)2D3, which is a vital regulator of calcium and phosphorus homeostasis. In humans, and possibly other vertebrates, 25(OH)D3 is also taken into the cells of many other organs possessing vitamin D3 receptors, including the immune system, where intracellular conversion to 1,25(OH)2D3 takes place (Hossein‐nezhad & Holick, 2013). Within the cells, 1,25(OH)2D3 has paracrine and autocrine functions (Björn, 2008).
Vitamin D3 is utilized by almost all vertebrate species studied (Björn, 2008), and the formation of vitamin D3 via 7‐DHC photoconversion is an ancient process which has been conserved through evolution. Most vertebrates are able to utilize pre‐formed vitamin D3 from the diet, which has enabled many species of reptiles to be maintained in captivity without UVb lighting but with dietary supplementation of vitamin D3. The first successful use of a fluorescent tube emitting UVb for reptile vitamin D3 synthesis was described by Laszlo (1969).
Since then, cutaneous synthesis of vitamin D3 under artificial UVb radiation has been demonstrated in several diurnal reptile species (Acierno, Mitchell, Roundtree, & Zachariah, 2006; Allen, Oftedal, & Horst, 1995; Bernard, Allen, & Ullrey, 1997; Ferguson et al., 2003, 2009; Gillespie et al., 2000; Hibma, 2004; Hoby et al., 2010; Kroenlein, Zimmerman, Saunders, & Holladay, 2011; Oonincx, Stevens, van den Borne, van Leeuwen, & Hendriks, 2010; Selleri & Di Girolamo, 2012), but also in crepuscular and nocturnal species (Acierno et al., 2008; Carman, Ferguson, Gehrmann, Chen, & Holick, 2000; Wangen, Kirchenbaum, & Mitchell, 2013). Most of these studies did not describe the UVb intensity and spectral distribution received by the subjects. The spectral power distribution of the light source determines the resulting photoproducts (MacLaughlin, Anderson, & Holick, 1982). The phosphor blend and transmission qualities of the outer glass tube from a UVb‐emitting fluorescent lamp determine its spectral power distribution and hence its vitamin D3 forming potential.
    loading  Loading Related Articles